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Pharmocokinetics > Liver disease and drug handling > Flashcards

Liver disease and drug handling Flashcards

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1
Q

metabolic reactions are either what phases?

A

Phase 1/ 2

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2
Q

Example of phase 1 reactions

A

Oxidation
Hydroxylation
Dealkylation
Deamination
Hydrolysis

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3
Q

Is phase 1 reactions anabolic/ catabolic?

A

catabolic —> breaking down of drug

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4
Q

Is phase 2 reactions anabolic/ catabolic?

A

anabolic : (conjugation)

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5
Q

Aspirin metabolic reactions : phase 1/phase 2

A

Phase 1 creates salicylic acid and Phase 2 creates a water-soluble molecule for excretion

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6
Q

what phase (1/2) drug reactions are affected more by increase in age?

A

Phase 1 drug reactions affected more than Phase 2

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7
Q

renal function can lead to reduced excretion of drugs. how? some factors

A

renal blood flow, filtration, renal mass decrease with age
Co-morbidities contribute to this decline

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8
Q

prothrombin time define:

A

how long it takes for clot to form

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9
Q

rifampicin induces what enzyme?

A

CYP2C9

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10
Q

Omeprazole inhibits what enzyme?

A

CYPC219

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11
Q

Omeprazole by inhibiting CYP2C19 this has what effect on clopidogrel?

A

prevents the production of active metabolite of clopidogrel

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12
Q

Rifampicin induces and enzyme. This has what effect on warfarin?

A

reduces anti-coagulant effect of warfarin

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13
Q

Liver metabolises?

A

carbohydrates (glycogen)
protein
lipids

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14
Q

Example of causes of liver disease?

A

alcohol, obesity, viral hepatitis

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15
Q

Stages of liver damage

A

healthy liver –> liver steatosis –> fibrosis liver —> cirrhosis liver –> liver cancer

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16
Q

wilsons disease is?

A

inherited disorder- accumulation of copper

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17
Q

Hemochromatosis disease is?

A

inherited disorder- Accumulation of iron

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18
Q

Examples of unusual cases that cause liver disease

A

tropical infections
TB
syphilis
lymphoma

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19
Q

example of drug-induced liver injury : DILI

A

Paracetamol
NSAID
Antidepressants

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20
Q

steps of drug-induced liver injury : DILI (detail)

A
  1. Inhibition of mitochondrial function–> preventing fatty acid metabolism, & accumulation of lactate & reactive oxygen species
  2. Disruption of bile canalicular transport mechanisms
  3. Disruption of intracellular homeostasis
  4. Formation of non-functioning adducts which may then lead to
    …presentation on the surface of hepatocytes as new immunogens (attacked by T-cells)
  5. Induction of apoptosis
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21
Q

steps of drug-induced liver injury : DILI ( simplified)

A
  1. Mitochondrial impairment
  2. Inhibition of biliary efflux
  3. Lysosome impairment
  4. Reactive metabolites
  5. Endoplasmic reiticulum stress
  6. Immune system
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22
Q

Drug- induced liver injury can either be:

A

intrahepatic
extrahepatic

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23
Q

intrahepatic define:

A

involving hepatocytes

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24
Q

extrahepatic define:

A

outside hepatocytes

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25
signs of intrahepatic DILI
often an immune-mediated response to a drug May be asymptomatic and may be associated with features of drug hypersensitivity e.g: skin,rash,fever
26
symptoms of intrahepatic DILI
Nausea, vomiting, anorexia, jaundice, right upper quadrant pain
27
signs of extrahepatic DILI
Jaundice, itching (due to accumulation of bile salts)
28
Extrahepatic DILI also called? What is it?
Also called cholestasis Reflects the inability of liver to remove bile from body due to blocked biliary ducts
29
Symptoms of extrahepatic DILI
May be asymptomatic
30
Intrahepatic vs extrahepatic
Intrahepatic = often an immune-mediated response to a drug Extrahepatic = reflects the inability of liver to remove bile from body due to blocked biliary ducts
31
Why might a patient experience disorientation/ confusion from DILI?
Liver is unable to get rid of toxic metabolites which can cause them to be confused
32
Liver function test: for hepatocellular damage
ALT AST
33
Liver function test: choleostasis, impair conjugation or biliary obstruction
Bilirubin ALP
34
Liver function test: synthetic function
PT Albumin
35
Liver function test: choleostasis or biliary obstruction
GGT Bile acids 5- nucleotides
36
AST ? Present also where?
Aspartate aminotransferase Present in the heart, muscle, kidney, brain
37
ALP? Present also where?
Alkaline phosphatase Present in placenta, bone
38
ALT? Present also where?
Alanine aminotransferase More specific to the liver
39
GGT? Present also where?
Gamma-glutamyltransferase Present in kidney, pancreas, heart, brain - chronic ethanol consumption
40
Raised ALP but normal GGT/ and or bilirubin, indicates?
Increased bone turnover/ vitamin D deficiency / bone fractures
41
Amino transferases are?
Enzymes contained in hepatocytes that leak into blood when cells are damaged
42
Raised ALT/ ATP indicates?
Hepatic
43
Raised ALT/ AST indicates?
Viral hepatitis - specific for liver injury + good marker for acute liver injury
44
Raised AST/ ALT indicates?
Alcohol liver disease/ NAFLD / cirrhosis - but also raised in myocardial infarction/ burns / trauma
45
Raised ALP / GGT and /or bilirubin
Cholestatic (Gall stones blocking the bile duct / induced medication)
46
Low albumin levels indicates?
Reduced synthetic function of the liver
47
Raised PT/ INR indicates?
prolonged clotting and reduced synthetic function in context of liver disease
48
Albumin levels can be low by other causes, examples?
Malnutrition, sepsis
49
What should be excused as the cause of a prolonged PT?
Vitamin K deficiency
50
Prothrombin time indicator of?
Acute and chronic liver disease
51
What treats coagulation factors?
Prothrombin
52
% Of cardiac output that passes through the liver?
20%
53
Liver metabolism can produce what? (Negative)
Toxic metabolites
54
Paracetamol metabolism
Phase 1 metabolism: by CYP450 isoforms to form NAPQI - NAPQI detoxifies through conjugation with glutathione Phase 2: metabolism = conjugation with glucoronide, sulphate - since non-toxic metabolites = elimination via kidneys
55
Phase 2: metabolism = conjugation with glucoronide, sulphate of paracetamol is eliminated via the kidneys. Why?
Non-toxic metabolite
56
If paracetamol taken in overdose, what happens in metabolism?
Paracetamol into phase 2 metabolism becomes saturated = more goes into phase I metabolism = more NAPQI formation = more hepatotoxic and nephrotoxic ( can't be eliminated via kidneys)
57
Dose - related toxicity is what type of ADR/ adverse drug reaction?
Type A ( augmented)
58
How can NAPQI cause renal failure?
Bind renal cells
59
NAPQI is highly reactive. This can have what effect?
Oxidises key enzymes causing cell death
60
What is given for paracetamol overdose? And mechanism.
N acetyl cysteine (NAC) Replenishes glutathione to get rid of excess NAPQI So it can carry on to phase 2 to be eliminated in the kidneys
61
Unpredictable, 'idiosyncratic' is what type of ADR?
Type B (bizarre)
62
Excessive drinking of alcohol leads to metabolic tolerance and increased levels of acetaldenyde. How?
Acetyladehyde dehydrogenase becomes fully saturated with alcohol leading to buildup of acetyladehyde
63
Chronic exposure to drug is what type of ADR?
Type C
64
Why avoid opioids in liver failure?
Central depressant action in patients with hepatic encephalopathy
65
Why avoid diuretics in liver failure?
Dehydration= Increased risk of hepatic encephalopathy
66
Why avoid warfarin in liver failure?
Enhances effects
67
Why avoid NSAIDs in liver failure?
Increased risk of bleeding
68
Why avoid oral hypoglycaemics in liver failure?
Loss of glucose homeostasis Increased risk of lactic acidosis
69
Why avoid ACE inhibitors in liver failure?
Hepatorenal failure
70
Drugs to avoid in liver failure : examples
Warfarin opioids Oral hypoglycaemics Ace inhibitors Diuretics NSAIDs
71
Ammonia toxin accumulating in blood =
Hepatic encephalopathy
72
DILI: Methotrexate can cause what type of liver damage?
Fibrosis
73
DILI: paracetamol can cause what type of liver damage?
Acute hepatic necrosis

Pharmocokinetics (22 decks)

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